Nagayama T, Yoshida M, Suzuki-Kusaba M, Hisa H, Kimura T, Satoh S
Department of Pharmacology, Pharmaceutical Institute, Tohoku University, Aobayama, Sendai, Japan.
Eur J Pharmacol. 1998 Jul 24;353(2-3):169-76. doi: 10.1016/s0014-2999(98)00408-7.
We examined whether high conductance Ca2+-activated K+ (BK(Ca)) channels are involved in the modulatory action of nitric oxide (NO) on the secretion of adrenal catecholamines in response to splanchnic nerve stimulation and acetylcholine in anesthetized dogs. The NO donor 3-(2-hydroxy-1-methyl-2-nitrosohydrazino)-N-methyl-1-propanamin e (NOC 7), the BK(Ca) channel blocker charybdotoxin and acetylcholine were administered intraarterially (i.a.) into the adrenal gland. NOC 7 infusion (2 microg min(-1)) inhibited increases in catecholamine output induced by splanchnic nerve stimulation (1-3 Hz) and acetylcholine (0.75-3 microg). Charybdotoxin infusion (100 ng min(-1)) did not affect increases in catecholamine output induced by splanchnic nerve stimulation and acetylcholine. Charybdotoxin blocked the NOC 7-induced inhibition of increases in catecholamine output induced by splanchnic nerve stimulation but not by acetylcholine. These results suggest that NO may inhibit the secretion of adrenal catecholamines induced by splanchnic nerve stimulation through activation of BK(Ca) channels.
